Continuing development of the Virginia Tech campus is increasing downstream flooding and water quality problems. To address these problems, the University has proposed the construction of a stormwater management facility to control the quantity and quality of stormwater releases to Strouble Creek, a tributary of the New River. The overall goal of this project is to design a stormwater management facility proposed for the Virginia-Maryland College of Veterinary Medicine at Virginia Tech in Blacksburg, Virginia that will reduce present and anticipated downstream flooding and water quality problems. Specific objectives of the project are: * control of flooding in lower areas by reducing the peak discharge while disturbing existing wetlands as little as possible, * address removal of major NPS pollutants such as total phosphorus (TP), total nitrogen (TN), metals, organic compounds related to petroleum and gasoline, and suspended sediment (SS) from stormwater runoff, and * design of a dam system that is able to withstand all driving forces and constructed in accordance with governing regulations. The design requirement to limit wetland disturbance below one acre was maintained. The requirement set by officials of Virginia Tech is based on the Nationwide Permit 26 of the Wetland Regulations. An individual permit process is thus avoided. Considering this demand, however, the freedom of the stormwater management facility design was significantly restricted. Resulting from the previous restrictions mentioned, the facility will include two ponds in series - a lower, dry pond and an upper, wet pond. The stormwater management system is designed to reduce the peak discharge. The dry pond is designed to detain water only for a short period of time, as opposed to the wet pond which is designed to retain water, thereby maintaining a permanent pool of water, and to change the characteristics of runoff. The wet pond was chosen to be of an Extended Detention wetland type. Aspects such as the availability of suitable area and detention volume governed the decision to make use of this type of stormwater wetland. The constraint on a maximum possible water surface elevation due to the Veterinary School1s road embankment, which crest elevation is at 2023 ft, was considered in the design. The stormwater management facility was designed to meet water quantity control requirements and to address water quality benefits. Storm water management regulations intending to mitigate the adverse effects of land development to streams and waterways were met. Requirements to limit peak discharges from 2-year and 10-year events to existing discharge levels were achieved. Several outlet structures for each of the ponds were investigated. The structures proposed are a perforated riser/broad-crested weir for the wet pond and a proportional weir for the dry pond. They were chosen as a result of analyses on hydraulic performance, maximum water surface elevations, drawdown times, peak discharge rates, and pollutant removal capabilities. The average pollutant removal capability of 75% of TSS, 45% TP, and 25% TN for an extended stormwater wetland, as found in the literature, is expected to be lower for the proposed facility, since the wetland-to-watershed-area ratio is considerably smaller (0.22%) than the required minimum ratio of 1%. However, other suggested desirable parameter for extended detention wetland systems such as required treatment volume, effective flow path length, and dry weather water balance will be maintained. The structural design of the dams was based on experience and research data. The dams are designed to consist of two zones, shell and core. The core extends as a cutoff trench 4 feet below the ground surface. Additionally, toe drain trenches and anti-seep collars along the pipe where penetrating the dam will be placed to collect and reduce seepage, respectively. Special considerations toward seepage problems were taken into account for both dams by placing a cutoff trench and a toe drain trench. Note: The appendix of this project report contains four AutoCAD files, that can only be viewed using AutoCAD. / Master of Engineering

<p>2-Methoxyestradiol (2-ME), a metabolite of 17β-estradiol, is a potent antitumor and antiangiogenesis agent in vitro and in vivo. This study aimed to investigate the effects of 2-ME on human cervical and endometrial cancers in vitro and in vivo. Human cervical cancer HeLaS3 cells, endometrial cancer HEC-1-A and RL-95-2 cells, and severe combined immune deficient (SCID) mice were used. On cervical cancer HeLaS3 cells, 2-ME inhibited the cell growth which is accompanied by apoptosis via iNOS pathway and by G₂/M cell cycle arrest. 2-ME had slight effects on normal cervical epithelial cells. In vivo on SCID mice, 2-ME (75 mg/kg p.o.) inhibited the growth of human cervical carcinoma by 34% (p < 0.05) and showed slight side effects to liver and spleen. On human endometrial cancer cells (HEC-1-A and RL-95-2 cells), 2-ME inhibited the growth by blocking cell cycle progress in S- and G₂/M-phase in both cell types, and by inducing apoptosis in HEC-1-A cells and by causing necrosis in RL-95-2 cells. 2-ME had no effects on normal endometrial cells. The apoptotic effect, in HEC-1-A cells, was prevented by iNOS-inhibitor 1400W and eliminated by Caspase-inhibitor Z-VAD-FMK. The necrosis, on RL-95-2 cells, was due to a severe disruption of the mitochondrial membrane potential. Unfortunately, 2-ME had no significant effects on endometrial cancer xenografts. It showed slight toxicity to liver, spleen and proliferative effect on uterus. In conclusion, 2-ME inhibits the growth of human cervical and endometrial cancer cells in vitro. However, a weaker anti-tumor effect was observed in our animal model and 2-ME was slightly toxic to liver and spleen. Considering the proliferative effect on uterus, 2-ME might not be a suitable therapeutic agent in gynecological tumors.</p>

2-Methoxyestradiol (2-ME), a metabolite of 17β-estradiol, is a potent antitumor and antiangiogenesis agent in vitro and in vivo. This study aimed to investigate the effects of 2-ME on human cervical and endometrial cancers in vitro and in vivo. Human cervical cancer HeLaS3 cells, endometrial cancer HEC-1-A and RL-95-2 cells, and severe combined immune deficient (SCID) mice were used. On cervical cancer HeLaS3 cells, 2-ME inhibited the cell growth which is accompanied by apoptosis via iNOS pathway and by G2/M cell cycle arrest. 2-ME had slight effects on normal cervical epithelial cells. In vivo on SCID mice, 2-ME (75 mg/kg p.o.) inhibited the growth of human cervical carcinoma by 34% (p &lt; 0.05) and showed slight side effects to liver and spleen. On human endometrial cancer cells (HEC-1-A and RL-95-2 cells), 2-ME inhibited the growth by blocking cell cycle progress in S- and G2/M-phase in both cell types, and by inducing apoptosis in HEC-1-A cells and by causing necrosis in RL-95-2 cells. 2-ME had no effects on normal endometrial cells. The apoptotic effect, in HEC-1-A cells, was prevented by iNOS-inhibitor 1400W and eliminated by Caspase-inhibitor Z-VAD-FMK. The necrosis, on RL-95-2 cells, was due to a severe disruption of the mitochondrial membrane potential. Unfortunately, 2-ME had no significant effects on endometrial cancer xenografts. It showed slight toxicity to liver, spleen and proliferative effect on uterus. In conclusion, 2-ME inhibits the growth of human cervical and endometrial cancer cells in vitro. However, a weaker anti-tumor effect was observed in our animal model and 2-ME was slightly toxic to liver and spleen. Considering the proliferative effect on uterus, 2-ME might not be a suitable therapeutic agent in gynecological tumors.